The function of the JNK signaling pathway in cornea: recent advances

Yan Xie1, Kuangqi Chen2, Dongjie Song3

  • 1Shengzhou People's Hospital (Shengzhou Branch of the First Affiliated Hospital of Zhejiang University School of Medicine, the Shengzhou Hospital of Shaoxing University), Shaoxing, China; Department of Ophthalmology, the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.

PubMed

Insights

The c-Jun N-terminal kinase (JNK) signaling pathway is crucial for corneal health and disease. Targeting JNK offers potential treatments for various corneal disorders like keratitis and dry eye disease.

Area of Science:

  • Ophthalmology
  • Molecular Biology
  • Cell Biology

Background:

  • The c-Jun N-terminal kinase (JNK) signaling pathway plays a critical role in maintaining corneal homeostasis.
  • Aberrant JNK activation is implicated in the pathogenesis of several corneal diseases, including keratitis, corneal dystrophy, and dry eye disease.
  • JNK signaling influences key cellular processes such as apoptosis, inflammation, fibrosis, and wound healing in the cornea.

Purpose of the Study:

  • To provide a systematic overview of the JNK signaling pathway in the cornea.
  • To highlight the role of JNK signaling in the progression of corneal diseases.
  • To explore potential therapeutic strategies targeting JNK for corneal conditions.

Main Methods:

  • This is a review article, synthesizing existing research on JNK signaling in the cornea.
  • Literature search and analysis of studies investigating JNK's role in corneal pathophysiology.
  • Examination of JNK's involvement in specific corneal disorders and its response to therapeutic interventions.

Main Results:

  • JNK signaling is activated by inflammatory cytokines and modulates corneal cell apoptosis, inflammation, fibrosis, and wound healing.
  • In keratitis, JNK activation exacerbates inflammation and injury.
  • In corneal dystrophy, JNK activation promotes pathogenic factor deposition, while inhibition aids wound healing.
  • In dry eye disease, hypertonicity induces apoptosis and inflammation via JNK modulation.

Conclusions:

  • JNK signaling is a pivotal regulator of corneal homeostasis and pathology.
  • Dysregulated JNK signaling contributes significantly to various corneal diseases.
  • Targeting JNK signaling presents a promising therapeutic avenue for improving outcomes in corneal diseases by regulating metabolism, inflammation, and wound healing.

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